L’hémodynamique pulmonaire au cours de l’exercice musculaire chez les bronchiteux chroniques

Weitzenblum, E; Vandevenne, A; Hirth, Christian; Parini, J.; Roeslin, N; Oudet, P

doi:10.1159/000193021

Cited by 11 publications

(13 citation statements)

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“…With regard to resting blood gas tensions, the reason for this difference might be that remodelling of pulmonary arteries can occur before significant hypoxaemia is evident. The lack of correlation between pulmonary haemodynamic parameters and both TL,CO and capillary volume does not suggest a primary effect of destruction of the capillary bed on the development of PH, in agreement with results from human and experimental animal studies [25][26][27][28].…”

Section: Discussionsupporting

confidence: 85%

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Relationship between exercise desaturation and pulmonary haemodynamics in COPD patients

Christensen¹

2004

European Respiratory Journal

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Pulmonary hypertension (PH) in patients with chronic obstructive pulmonary disease (COPD) has traditionally been explained as an effect of hypoxaemia. Recently, other mechanisms, such as arterial remodelling caused by inflammation, have been suggested. The aim of this study was to investigate whether exercise-induced PH (EIPH) could occur without concurrent hypoxaemia, and whether exercise-induced hypoxaemia (EIH) was regularly accompanied by increased pulmonary artery pressure or pulmonary vascular resistance index (PVRI).Pulmonary haemodynamics in 17 patients with COPD of varying severity, but with no or mild hypoxaemia at rest, were examined during exercise equivalent to the activities of daily living (ADL) and exhaustion.EIPH occurred in 65% of the patients during ADL exercise. Pulmonary arterial pressure during exercise was negatively correlated with arterial oxygen tension, but EIPH was not invariably accompanied by hypoxaemia. Conversely, EIPH was not found in all patients with EIH. The resting PVRI was negatively correlated with arterial oxygen tension during ADL exercise, but an elevated PVRI without EIH occurred in 35% of the patients.In conclusion, exercise-induced pulmonary hypertension occurred during exercise equivalent to the activities of daily living in chronic obstructive pulmonary disease patients with no or mild hypoxaemia at rest. Although pulmonary artery pressure and arterial oxygen tension were negatively correlated during exercise, a consistent relationship between hypoxaemia and pulmonary hypertension could not be demonstrated. This may indicate that mechanisms other than hypoxaemia contribute significantly in the development of pulmonary hypertension in these patients. Eur Respir J 2004; 24: 580-586

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Section: Discussionsupporting

confidence: 85%

“…WEITZENBLUM et al [26] found a significant partial correlation between Ppa and Pa,O 2 (at constant CI) in COPD patients during supine cycling, indicating an effect of hypoxaemia on the PVRI. However, PH has primarily been associated with resting Pa,O 2 of v y8 kPa [20].…”

Section: Discussionmentioning

confidence: 96%

Relationship between exercise desaturation and pulmonary haemodynamics in COPD patients

Christensen¹

2004

European Respiratory Journal

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“…In most of the patients (54 of the 94), measurements could also be obtained during the last minute of a 7 min steady-state exercise performed on an ergometric bicycle, in the supine position; the load being 40 W, or less in patients who were too breathless. The modalities of exercise testing have been described previously [23].…”

Section: Methodsmentioning

confidence: 99%

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Chaouat¹,

Weitzenblum²,

Kessler³

et al. 1997

Eur Respir J

155

102

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It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia.We have investigated the relationships between pulmonary function data, sleeprelated desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O 2 therapy (daytime arterial oxygen tension (Pa,O 2 ) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending ≥30% of the recording time with a transcutaneous O 2 saturation <90%. An obstructive sleep apnoea syndrome was excluded by polysomnography.Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O 2 (8.4±0.6 vs 8.4±0.4 kPa (63±4 vs 63±3 mmHg)) but arterial carbon dioxide tension (Pa,CO 2 ) was higher in Group 1 (6.0±0.7 vs 5.3±0.5 kPa (45±5 vs 40±4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6±0.7 vs 2.5±0.6 kPa (19±5 vs 19±4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension.It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension. Eur Respir J 1997; 10: 1730-1735 The worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease (COPD) has been documented since the early 1960s [1], and has since been confirmed by polysomnographic studies [2,3], which have included continuous monitoring of oxygen saturation from the late 1970s [4][5][6][7][8][9][10]. It must be emphasized that most of these studies have included patients with severe COPD exhibiting marked daytime hypoxaemia. Is sleep-related hypoxaemia present in patients with less severe COPD with mild or absent daytime hypoxaemia? Several studies of the literature [11][12][13] have shown that a relatively high percentage of these COPD patients exhibit significant nocturnal hypoxaemia, which naturally raises the question: Does this hypoxaemia, limited to sleep, deserve treatment with nocturnal oxygen? Such a treatment could be justified if nocturnal hypoxaemia had deleterious effects on life expectancy, which is rather controversial [14,15], and on pulmonary haemodynamics. It has been hypothesized [16,17] that isolated nocturnal hypoxaemia, occurring in patients without significant daytime hypoxaemia, could lead to permanent (daytime) pulmonary hypertension, but this hypothesis has not, so...

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“…Hipoksiyle oluşan pulmoner vazokonstriksiyon ve pulmo-ner damar direnci artmasında anatomik ve vazomotor mekanizmalar rol oynamaktadır (8,9,10,19,201…”

Section: )unclassified

“…Daha önce yapılan yayınlarda pulmoner hipertansiyonlu olgularda zorlu ekspirasyonun birinci saniyesinde atılan volü-mün düşük olduğu bildirilmiştir (8,9,19).…”

unclassified

Kroni̇k Obstrükti̇f Akci̇ğer Hastaliğinda Pulmoner Hemodi̇nami̇ Ve Akci̇ğer Mekani̇kleri̇

Gülseren;BARTU¹

1994

Ankara Üniversitesi Tıp Fakültesi Mecmuası

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L’hémodynamique pulmonaire au cours de l’exercice musculaire chez les bronchiteux chroniques

Cited by 11 publications

References 0 publications

Relationship between exercise desaturation and pulmonary haemodynamics in COPD patients

Relationship between exercise desaturation and pulmonary haemodynamics in COPD patients

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Kroni̇k Obstrükti̇f Akci̇ğer Hastaliğinda Pulmoner Hemodi̇nami̇ Ve Akci̇ğer Mekani̇kleri̇

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